Alzheimer’s disease is the most common form of dementia. It is characterized by betaamyloid
peptide fibrils which are extracellular deposition of a specific protein, accompanied by extensive
neuroinflammation. Various studies show the presence of a number of inflammation markers in
the AD brain: elevated inflammatory cytokines and chemokines, and an accumulation of activated microglia
in the damaged regions. NF-κB is a family of redox sensitive transcriptional factors, and it is
known that NF-κB has binding sites in the promoter region of the genes involved in amyloidogenesis
and inflammation. Long-term use of non-steroidal anti-inflammatory drugs prevents progression of
AD and delays its onset, suggesting that there is a close correlation between NF-κB and AD pathogenesis.
This study aims to (1) assess the association between NF-κB activity and AD through discussion
of a variety of experimental and clinical studies on AD and (2) review treatment strategies designed
to treat or prevent AD with NF-κB inhibitors.
Keywords: Alzheimer’s disease, amyloidogenesis, Beta-amyloid, neuroinflammation, nuclear factor kappa B, nuclear factor
kappa B inhibitor.
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